A Twenty-First Century Cancer Epidemic Caused by Obesity: The Involvement of Insulin, Diabetes, and Insulin-Like Growth Factors
Figure 1
Insulin homeostasis in normal and obese individuals. In normal individuals, the postprandial increase in blood glucose concentration stimulates the beta cells in the Islets of Langerhans of the pancreas to release insulin (a). Insulin stimulates the uptake of glucose by liver and muscle cells and conversion of glucose to the energy store glycogen primarily in the liver and in skeletal muscle. The decrease in glucose levels in the blood of fasted individuals stimulates the alpha cells of the Islets of Langerhans in the pancreas to release glucagon. Glucagon stimulates the conversion of glycogen to glucose by glycogenolysis. In obese individuals, adipocytes in adipose tissue release nonesterified or free fatty acids (FFAs) energy into the circulation (b). The hepatic portal vein provides a direct conduit of free fatty acids from visceral adipose tissue to the liver. The high serum concentrations of nonesterified fatty acids force tissues to prioritise their oxidation as an energy source which prevents glucose uptake. Hence, the obese individual is resistant to the high levels of insulin secreted after a meal and blood glucose levels remain chronically high regardless of the fed state of the obese individual. The pancreas continues to secrete insulin in response to the high blood glucose levels. The obese individual manifests hyperglycaemia and hyperinsulinaemia.
